Mohammad Shafi Kuchay1, Sunil Kumar Mishra2, Beena Bansal2, Khalid Jamal Farooqui2, Lalitha Sekhar3, Ambrish Mithal2. 1. Division of Endocrinology and Diabetes, Medanta-The Medicity, Sector 38, Gurgaon, Haryana, 122001, India. drshafikuchay@gmail.com. 2. Division of Endocrinology and Diabetes, Medanta-The Medicity, Sector 38, Gurgaon, Haryana, 122001, India. 3. Division of Internal Medicine, Medanta-The Medicity, Sector-38, Gurgaon, Haryana, 122001, India.
Abstract
INTRODUCTION: Glucocorticoids are regarded as first-line therapy in the management of hypercalcemia associated with sarcoidosis. However, prolonged glucocorticoid therapy leads to metabolic abnormalities, Cushingoid habitus, and impairment of bone health. This study demonstrates the efficacy and glucocorticoid-sparing effect of zoledronic acid in sarcoid hypercalcemia. METHODS: We present three patients with sarcoid hypercalcemia. They were successfully managed with oral glucocorticoids for many months. However, all patients developed adverse effects of glucocorticoids. When tapering of glucocorticoids was attempted, hypercalcemia recurred. Zoledronic acid was administered in order to control hypercalcemia and to allow tapering of glucocorticoids. RESULTS: Following zoledronic acid administration, serum calcium level normalised and glucocorticoids could be discontinued in all the three patients. Normocalcemia was maintained for an average of 18 months after a single infusion. Sarcoidosis remained in remission in all the three patients. CONCLUSION: Zoledronic acid should be studied as a potential first-line agent for sarcoid hypercalcemia. Furthermore, disease-modifying effects of zoledronic acid in sarcoidosis should be investigated.
INTRODUCTION: Glucocorticoids are regarded as first-line therapy in the management of hypercalcemia associated with sarcoidosis. However, prolonged glucocorticoid therapy leads to metabolic abnormalities, Cushingoid habitus, and impairment of bone health. This study demonstrates the efficacy and glucocorticoid-sparing effect of zoledronic acid in sarcoid hypercalcemia. METHODS: We present three patients with sarcoid hypercalcemia. They were successfully managed with oral glucocorticoids for many months. However, all patients developed adverse effects of glucocorticoids. When tapering of glucocorticoids was attempted, hypercalcemia recurred. Zoledronic acid was administered in order to control hypercalcemia and to allow tapering of glucocorticoids. RESULTS: Following zoledronic acid administration, serum calcium level normalised and glucocorticoids could be discontinued in all the three patients. Normocalcemia was maintained for an average of 18 months after a single infusion. Sarcoidosis remained in remission in all the three patients. CONCLUSION:Zoledronic acid should be studied as a potential first-line agent for sarcoid hypercalcemia. Furthermore, disease-modifying effects of zoledronic acid in sarcoidosis should be investigated.